TY  - JOUR
AU  - McCubrey, James A
AU  - Steelman, Linda S
AU  - Abrams, Stephen L
AU  - Misaghian, Negin
AU  - Chappell, William H
AU  - Baesecke, Joerg
AU  - Nicoletti, Ferdinando
AU  - Libra, Massimo
AU  - Ligresti, Giovanni
AU  - Stivala, Franca
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Montalto, Giuseppe
AU  - Cervello, Melchiorre
AU  - Laidler, Piotr
AU  - Bonati, Antonio
AU  - Evangelisti, Camilla
AU  - Cocco, Lucio
AU  - Martelli, Alberto M
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1183
AB  - An area of therapeutic interest in cancer biology and treatment is targeting the cancer stem cell, more appropriately referred to as the cancer initiating cell (CIC). CICs comprise a subset of hierarchically organized, rare cancer cells with the ability to initiate cancer in xenografts in genetically modified murine models. CICs are thought to be responsible for tumor onset, self-renewal/maintenance, mutation accumulation and metastasis. CICs may lay dormant after various cancer therapies which eliminate the more rapidly proliferating bulk cancer (BC) mass. However, CICs may remerge after therapy is discontinued as they may represent cells which were either intrinsically resistant to the original therapeutic approach or they have acquired mutations which confer resistance to the primary therapy. In experimental mouse tumor transplant models, CICs have the ability to transfer the tumor to immunocompromised mice very efficiently while the BCs are not able to do so as effectively. Often CICs display increased expression of proteins involved in drug resistance and hence they are intrinsically resistant to many chemotherapeutic approaches. Furthermore, the CICs may be in a suspended state of proliferation and not sensitive to common chemotherapeutic and radiological approaches often employed to eliminate the rapidly proliferating BCs. Promising therapeutic approaches include the targeting of certain signal transduction pathways (e.g., RAC, WNT, PI3K, PML) with small molecule inhibitors or targeting specific cell-surface molecules (e.g., CD44), with effective cytotoxic antibodies. The existence of CICs could explain the high frequency of relapse and resistance to many currently used cancer therapies. New approaches should be developed to effectively target the CIC which could vastly improve cancer therapies and outcomes. This review will discuss recent concepts of targeting CICs in certain leukemia models.
T2  - Current Pharmaceutical Design
T1  - Targeting the Cancer Initiating Cell: The Ultimate Target for Cancer Therapy
IS  - 13
VL  - 18
EP  - 1795
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1183
ER  - 

@article{
author = "McCubrey, James A and Steelman, Linda S and Abrams, Stephen L and Misaghian, Negin and Chappell, William H and Baesecke, Joerg and Nicoletti, Ferdinando and Libra, Massimo and Ligresti, Giovanni and Stivala, Franca and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Montalto, Giuseppe and Cervello, Melchiorre and Laidler, Piotr and Bonati, Antonio and Evangelisti, Camilla and Cocco, Lucio and Martelli, Alberto M",
year = "2012",
abstract = "An area of therapeutic interest in cancer biology and treatment is targeting the cancer stem cell, more appropriately referred to as the cancer initiating cell (CIC). CICs comprise a subset of hierarchically organized, rare cancer cells with the ability to initiate cancer in xenografts in genetically modified murine models. CICs are thought to be responsible for tumor onset, self-renewal/maintenance, mutation accumulation and metastasis. CICs may lay dormant after various cancer therapies which eliminate the more rapidly proliferating bulk cancer (BC) mass. However, CICs may remerge after therapy is discontinued as they may represent cells which were either intrinsically resistant to the original therapeutic approach or they have acquired mutations which confer resistance to the primary therapy. In experimental mouse tumor transplant models, CICs have the ability to transfer the tumor to immunocompromised mice very efficiently while the BCs are not able to do so as effectively. Often CICs display increased expression of proteins involved in drug resistance and hence they are intrinsically resistant to many chemotherapeutic approaches. Furthermore, the CICs may be in a suspended state of proliferation and not sensitive to common chemotherapeutic and radiological approaches often employed to eliminate the rapidly proliferating BCs. Promising therapeutic approaches include the targeting of certain signal transduction pathways (e.g., RAC, WNT, PI3K, PML) with small molecule inhibitors or targeting specific cell-surface molecules (e.g., CD44), with effective cytotoxic antibodies. The existence of CICs could explain the high frequency of relapse and resistance to many currently used cancer therapies. New approaches should be developed to effectively target the CIC which could vastly improve cancer therapies and outcomes. This review will discuss recent concepts of targeting CICs in certain leukemia models.",
journal = "Current Pharmaceutical Design",
title = "Targeting the Cancer Initiating Cell: The Ultimate Target for Cancer Therapy",
number = "13",
volume = "18",
pages = "1795",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1183"
}

McCubrey, J. A., Steelman, L. S., Abrams, S. L., Misaghian, N., Chappell, W. H., Baesecke, J., Nicoletti, F., Libra, M., Ligresti, G., Stivala, F., Maksimović-Ivanić, D., Mijatović, S., Montalto, G., Cervello, M., Laidler, P., Bonati, A., Evangelisti, C., Cocco, L.,& Martelli, A. M.. (2012). Targeting the Cancer Initiating Cell: The Ultimate Target for Cancer Therapy. in Current Pharmaceutical Design, 18(13).
https://hdl.handle.net/21.15107/rcub_ibiss_1183

McCubrey JA, Steelman LS, Abrams SL, Misaghian N, Chappell WH, Baesecke J, Nicoletti F, Libra M, Ligresti G, Stivala F, Maksimović-Ivanić D, Mijatović S, Montalto G, Cervello M, Laidler P, Bonati A, Evangelisti C, Cocco L, Martelli AM. Targeting the Cancer Initiating Cell: The Ultimate Target for Cancer Therapy. in Current Pharmaceutical Design. 2012;18(13):null-1795.
https://hdl.handle.net/21.15107/rcub_ibiss_1183 .

McCubrey, James A, Steelman, Linda S, Abrams, Stephen L, Misaghian, Negin, Chappell, William H, Baesecke, Joerg, Nicoletti, Ferdinando, Libra, Massimo, Ligresti, Giovanni, Stivala, Franca, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Montalto, Giuseppe, Cervello, Melchiorre, Laidler, Piotr, Bonati, Antonio, Evangelisti, Camilla, Cocco, Lucio, Martelli, Alberto M, "Targeting the Cancer Initiating Cell: The Ultimate Target for Cancer Therapy" in Current Pharmaceutical Design, 18, no. 13 (2012),
https://hdl.handle.net/21.15107/rcub_ibiss_1183 .

TY  - JOUR
AU  - Steelman, Linda S
AU  - Chappell, William H
AU  - Abrams, Stephen L
AU  - Kempf, C Ruth
AU  - Long, Jacquelyn M
AU  - Laidler, Piotr
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Stivala, Franca
AU  - Mazzarino, Maria C
AU  - Donia, Marco
AU  - Fagone, Paolo
AU  - Malaponte, Graziella
AU  - Nicoletti, Ferdinando
AU  - Libra, Massimo
AU  - Milella, Michele
AU  - Tafuri, Agostino
AU  - Bonati, Antonio
AU  - Baesecke, Joerg
AU  - Cocco, Lucio
AU  - Evangelisti, Camilla
AU  - Martelli, Alberto M
AU  - Montalto, Giuseppe
AU  - Cervello, Melchiorre
AU  - McCubrey, James A
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1302
UR  - https://www.aging-us.com/article/100296
AB  - Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described roles of these pathways in cancer stem cells, cellular senescence and aging will be evaluated. Controlling the expression of these pathways could ameliorate human health.
T2  - Aging-US
T1  - Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging
IS  - 3
VL  - 3
DO  - 10.18632/aging.100296
EP  - 222
ER  - 

@article{
author = "Steelman, Linda S and Chappell, William H and Abrams, Stephen L and Kempf, C Ruth and Long, Jacquelyn M and Laidler, Piotr and Mijatović, Sanja and Maksimović-Ivanić, Danijela and Stivala, Franca and Mazzarino, Maria C and Donia, Marco and Fagone, Paolo and Malaponte, Graziella and Nicoletti, Ferdinando and Libra, Massimo and Milella, Michele and Tafuri, Agostino and Bonati, Antonio and Baesecke, Joerg and Cocco, Lucio and Evangelisti, Camilla and Martelli, Alberto M and Montalto, Giuseppe and Cervello, Melchiorre and McCubrey, James A",
year = "2011",
abstract = "Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described roles of these pathways in cancer stem cells, cellular senescence and aging will be evaluated. Controlling the expression of these pathways could ameliorate human health.",
journal = "Aging-US",
title = "Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging",
number = "3",
volume = "3",
doi = "10.18632/aging.100296",
pages = "222"
}

Steelman, L. S., Chappell, W. H., Abrams, S. L., Kempf, C. R., Long, J. M., Laidler, P., Mijatović, S., Maksimović-Ivanić, D., Stivala, F., Mazzarino, M. C., Donia, M., Fagone, P., Malaponte, G., Nicoletti, F., Libra, M., Milella, M., Tafuri, A., Bonati, A., Baesecke, J., Cocco, L., Evangelisti, C., Martelli, A. M., Montalto, G., Cervello, M.,& McCubrey, J. A.. (2011). Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging. in Aging-US, 3(3).
https://doi.org/10.18632/aging.100296

Steelman LS, Chappell WH, Abrams SL, Kempf CR, Long JM, Laidler P, Mijatović S, Maksimović-Ivanić D, Stivala F, Mazzarino MC, Donia M, Fagone P, Malaponte G, Nicoletti F, Libra M, Milella M, Tafuri A, Bonati A, Baesecke J, Cocco L, Evangelisti C, Martelli AM, Montalto G, Cervello M, McCubrey JA. Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging. in Aging-US. 2011;3(3):null-222.
doi:10.18632/aging.100296 .

Steelman, Linda S, Chappell, William H, Abrams, Stephen L, Kempf, C Ruth, Long, Jacquelyn M, Laidler, Piotr, Mijatović, Sanja, Maksimović-Ivanić, Danijela, Stivala, Franca, Mazzarino, Maria C, Donia, Marco, Fagone, Paolo, Malaponte, Graziella, Nicoletti, Ferdinando, Libra, Massimo, Milella, Michele, Tafuri, Agostino, Bonati, Antonio, Baesecke, Joerg, Cocco, Lucio, Evangelisti, Camilla, Martelli, Alberto M, Montalto, Giuseppe, Cervello, Melchiorre, McCubrey, James A, "Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways in controlling growth and sensitivity to therapy-implications for cancer and aging" in Aging-US, 3, no. 3 (2011),
https://doi.org/10.18632/aging.100296 . .

TY  - JOUR
AU  - McCubrey, James A
AU  - Steelman, Linda S
AU  - Kempf, C Ruth
AU  - Chappell, William H
AU  - Abrams, Stephen L
AU  - Stivala, Franca
AU  - Malaponte, Graziella
AU  - Nicoletti, Ferdinando
AU  - Libra, Massimo
AU  - Baesecke, Joerg
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Montalto, Giuseppe
AU  - Cervello, Melchiorre
AU  - Cocco, Lucio
AU  - Martelli, Alberto M
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1252
AB  - Chemotherapy remains a commonly used therapeutic approach for many cancers. Indeed chemotherapy is relatively effective for treatment of certain cancers and it may be the only therapy (besides radiotherapy) that is appropriate for certain cancers. However, a common problem with chemotherapy is the development of drug resistance. Many studies on the mechanisms of drug resistance concentrated on the expression of membrane transporters and how they could be aberrantly regulated in drug resistant cells. Attempts were made to isolate specific inhibitors which could be used to treat drug resistant patients. Unfortunately most of these drug transporter inhibitors have not proven effective for therapy. Recently the possibilities of more specific, targeted therapies have sparked the interest of clinical and basic researchers as approaches to kill cancer cells. However, there are also problems associated with these targeted therapies. Two key signaling pathways involved in the regulation of cell growth are the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways. Dysregulated signaling through these pathways is often the result of genetic alterations in critical components in these pathways as well as mutations in upstream growth factor receptors. Furthermore, these pathways may be activated by chemotherapeutic drugs and ionizing radiation. This review documents how their abnormal expression can contribute to drug resistance as well as resistance to targeted therapy. This review will discuss in detail PTEN regulation as this is a critical tumor suppressor gene frequently dysregulated in human cancer which contributes to therapy resistance. Controlling the expression of these pathways could improve cancer therapy and ameliorate human health.
T2  - Journal of Cellular Physiology
T1  - Therapeutic Resistance Resulting From Mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Signaling Pathways
IS  - 11
VL  - 226
DO  - 10.1002/jcp.22647
EP  - 2781
ER  - 

@article{
author = "McCubrey, James A and Steelman, Linda S and Kempf, C Ruth and Chappell, William H and Abrams, Stephen L and Stivala, Franca and Malaponte, Graziella and Nicoletti, Ferdinando and Libra, Massimo and Baesecke, Joerg and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Montalto, Giuseppe and Cervello, Melchiorre and Cocco, Lucio and Martelli, Alberto M",
year = "2011",
abstract = "Chemotherapy remains a commonly used therapeutic approach for many cancers. Indeed chemotherapy is relatively effective for treatment of certain cancers and it may be the only therapy (besides radiotherapy) that is appropriate for certain cancers. However, a common problem with chemotherapy is the development of drug resistance. Many studies on the mechanisms of drug resistance concentrated on the expression of membrane transporters and how they could be aberrantly regulated in drug resistant cells. Attempts were made to isolate specific inhibitors which could be used to treat drug resistant patients. Unfortunately most of these drug transporter inhibitors have not proven effective for therapy. Recently the possibilities of more specific, targeted therapies have sparked the interest of clinical and basic researchers as approaches to kill cancer cells. However, there are also problems associated with these targeted therapies. Two key signaling pathways involved in the regulation of cell growth are the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways. Dysregulated signaling through these pathways is often the result of genetic alterations in critical components in these pathways as well as mutations in upstream growth factor receptors. Furthermore, these pathways may be activated by chemotherapeutic drugs and ionizing radiation. This review documents how their abnormal expression can contribute to drug resistance as well as resistance to targeted therapy. This review will discuss in detail PTEN regulation as this is a critical tumor suppressor gene frequently dysregulated in human cancer which contributes to therapy resistance. Controlling the expression of these pathways could improve cancer therapy and ameliorate human health.",
journal = "Journal of Cellular Physiology",
title = "Therapeutic Resistance Resulting From Mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Signaling Pathways",
number = "11",
volume = "226",
doi = "10.1002/jcp.22647",
pages = "2781"
}

McCubrey, J. A., Steelman, L. S., Kempf, C. R., Chappell, W. H., Abrams, S. L., Stivala, F., Malaponte, G., Nicoletti, F., Libra, M., Baesecke, J., Maksimović-Ivanić, D., Mijatović, S., Montalto, G., Cervello, M., Cocco, L.,& Martelli, A. M.. (2011). Therapeutic Resistance Resulting From Mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Signaling Pathways. in Journal of Cellular Physiology, 226(11).
https://doi.org/10.1002/jcp.22647

McCubrey JA, Steelman LS, Kempf CR, Chappell WH, Abrams SL, Stivala F, Malaponte G, Nicoletti F, Libra M, Baesecke J, Maksimović-Ivanić D, Mijatović S, Montalto G, Cervello M, Cocco L, Martelli AM. Therapeutic Resistance Resulting From Mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Signaling Pathways. in Journal of Cellular Physiology. 2011;226(11):null-2781.
doi:10.1002/jcp.22647 .

McCubrey, James A, Steelman, Linda S, Kempf, C Ruth, Chappell, William H, Abrams, Stephen L, Stivala, Franca, Malaponte, Graziella, Nicoletti, Ferdinando, Libra, Massimo, Baesecke, Joerg, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Montalto, Giuseppe, Cervello, Melchiorre, Cocco, Lucio, Martelli, Alberto M, "Therapeutic Resistance Resulting From Mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Signaling Pathways" in Journal of Cellular Physiology, 226, no. 11 (2011),
https://doi.org/10.1002/jcp.22647 . .

TY  - JOUR
AU  - Chappell, William H
AU  - Steelman, Linda S
AU  - Long, Jacquelyn M
AU  - Kempf, Ruth C
AU  - Abrams, Stephen L
AU  - Franklin, Richard A
AU  - Baesecke, Joerg
AU  - Stivala, Franca
AU  - Donia, Marco
AU  - Fagone, Paolo
AU  - Malaponte, Graziella
AU  - Mazzarino, Maria C
AU  - Nicoletti, Ferdinando
AU  - Libra, Massimo
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Montalto, Giuseppe
AU  - Cervello, Melchiorre
AU  - Laidler, Piotr
AU  - Milella, Michele
AU  - Tafuri, Agostino
AU  - Bonati, Antonio
AU  - Evangelisti, Camilla
AU  - Cocco, Lucio
AU  - Martelli, Alberto M
AU  - McCubrey, James A
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1300
AB  - The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Integral components of these pathways, Ras, B-Raf, PI3K, and PTEN are also activated/inactivated by mutations. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of these pathways can contribute to chemotherapeutic drug resistance, proliferation of cancer initiating cells (CICs) and premature aging. This review will evaluate more recently described potential uses of MEK, PI3K, Akt and mTOR inhibitors in the proliferation of malignant cells, suppression of CICs, cellular senescence and prevention of aging. Ras/Raf/MEK/ERK and Ras/PI3K/PTEN/Akt/mTOR pathways play key roles in the regulation of normal and malignant cell growth. Inhibitors targeting these pathways have many potential uses from suppression of cancer, proliferative diseases as well as aging.
T2  - Oncotarget
T1  - Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Inhibitors: Rationale and Importance to Inhibiting These Pathways in Human Health
IS  - 3
VL  - 2
DO  - 10.18632/oncotarget.240
EP  - 164
ER  - 

@article{
author = "Chappell, William H and Steelman, Linda S and Long, Jacquelyn M and Kempf, Ruth C and Abrams, Stephen L and Franklin, Richard A and Baesecke, Joerg and Stivala, Franca and Donia, Marco and Fagone, Paolo and Malaponte, Graziella and Mazzarino, Maria C and Nicoletti, Ferdinando and Libra, Massimo and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Montalto, Giuseppe and Cervello, Melchiorre and Laidler, Piotr and Milella, Michele and Tafuri, Agostino and Bonati, Antonio and Evangelisti, Camilla and Cocco, Lucio and Martelli, Alberto M and McCubrey, James A",
year = "2011",
abstract = "The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Integral components of these pathways, Ras, B-Raf, PI3K, and PTEN are also activated/inactivated by mutations. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of these pathways can contribute to chemotherapeutic drug resistance, proliferation of cancer initiating cells (CICs) and premature aging. This review will evaluate more recently described potential uses of MEK, PI3K, Akt and mTOR inhibitors in the proliferation of malignant cells, suppression of CICs, cellular senescence and prevention of aging. Ras/Raf/MEK/ERK and Ras/PI3K/PTEN/Akt/mTOR pathways play key roles in the regulation of normal and malignant cell growth. Inhibitors targeting these pathways have many potential uses from suppression of cancer, proliferative diseases as well as aging.",
journal = "Oncotarget",
title = "Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Inhibitors: Rationale and Importance to Inhibiting These Pathways in Human Health",
number = "3",
volume = "2",
doi = "10.18632/oncotarget.240",
pages = "164"
}

Chappell, W. H., Steelman, L. S., Long, J. M., Kempf, R. C., Abrams, S. L., Franklin, R. A., Baesecke, J., Stivala, F., Donia, M., Fagone, P., Malaponte, G., Mazzarino, M. C., Nicoletti, F., Libra, M., Maksimović-Ivanić, D., Mijatović, S., Montalto, G., Cervello, M., Laidler, P., Milella, M., Tafuri, A., Bonati, A., Evangelisti, C., Cocco, L., Martelli, A. M.,& McCubrey, J. A.. (2011). Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Inhibitors: Rationale and Importance to Inhibiting These Pathways in Human Health. in Oncotarget, 2(3).
https://doi.org/10.18632/oncotarget.240

Chappell WH, Steelman LS, Long JM, Kempf RC, Abrams SL, Franklin RA, Baesecke J, Stivala F, Donia M, Fagone P, Malaponte G, Mazzarino MC, Nicoletti F, Libra M, Maksimović-Ivanić D, Mijatović S, Montalto G, Cervello M, Laidler P, Milella M, Tafuri A, Bonati A, Evangelisti C, Cocco L, Martelli AM, McCubrey JA. Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Inhibitors: Rationale and Importance to Inhibiting These Pathways in Human Health. in Oncotarget. 2011;2(3):null-164.
doi:10.18632/oncotarget.240 .

Chappell, William H, Steelman, Linda S, Long, Jacquelyn M, Kempf, Ruth C, Abrams, Stephen L, Franklin, Richard A, Baesecke, Joerg, Stivala, Franca, Donia, Marco, Fagone, Paolo, Malaponte, Graziella, Mazzarino, Maria C, Nicoletti, Ferdinando, Libra, Massimo, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Montalto, Giuseppe, Cervello, Melchiorre, Laidler, Piotr, Milella, Michele, Tafuri, Agostino, Bonati, Antonio, Evangelisti, Camilla, Cocco, Lucio, Martelli, Alberto M, McCubrey, James A, "Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Inhibitors: Rationale and Importance to Inhibiting These Pathways in Human Health" in Oncotarget, 2, no. 3 (2011),
https://doi.org/10.18632/oncotarget.240 . .

TY  - CONF
AU  - Steelman, Linda S
AU  - Abrams, Stephen L
AU  - Chappell, William H
AU  - Martelli, Alberto M
AU  - Nicoletti, Ferdinando
AU  - Fagone, Paolo
AU  - Mazzarino, Clorinda
AU  - Malaponte, Graziella
AU  - Libra, Massimo
AU  - Stivala, Franca
AU  - Cervello, Melchiorre
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - McCubrey, James A
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1313
C3  - International Journal of Molecular Medicine
T1  - Sensitization of cancer stem cells based on inhibiting key signal transduction pathways
IS  - null
VL  - 28
EP  - S18
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1313
ER  - 

@conference{
author = "Steelman, Linda S and Abrams, Stephen L and Chappell, William H and Martelli, Alberto M and Nicoletti, Ferdinando and Fagone, Paolo and Mazzarino, Clorinda and Malaponte, Graziella and Libra, Massimo and Stivala, Franca and Cervello, Melchiorre and Mijatović, Sanja and Maksimović-Ivanić, Danijela and McCubrey, James A",
year = "2011",
journal = "International Journal of Molecular Medicine",
title = "Sensitization of cancer stem cells based on inhibiting key signal transduction pathways",
number = "null",
volume = "28",
pages = "S18",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1313"
}

Steelman, L. S., Abrams, S. L., Chappell, W. H., Martelli, A. M., Nicoletti, F., Fagone, P., Mazzarino, C., Malaponte, G., Libra, M., Stivala, F., Cervello, M., Mijatović, S., Maksimović-Ivanić, D.,& McCubrey, J. A.. (2011). Sensitization of cancer stem cells based on inhibiting key signal transduction pathways. in International Journal of Molecular Medicine, 28(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1313

Steelman LS, Abrams SL, Chappell WH, Martelli AM, Nicoletti F, Fagone P, Mazzarino C, Malaponte G, Libra M, Stivala F, Cervello M, Mijatović S, Maksimović-Ivanić D, McCubrey JA. Sensitization of cancer stem cells based on inhibiting key signal transduction pathways. in International Journal of Molecular Medicine. 2011;28(null):null-S18.
https://hdl.handle.net/21.15107/rcub_ibiss_1313 .

Steelman, Linda S, Abrams, Stephen L, Chappell, William H, Martelli, Alberto M, Nicoletti, Ferdinando, Fagone, Paolo, Mazzarino, Clorinda, Malaponte, Graziella, Libra, Massimo, Stivala, Franca, Cervello, Melchiorre, Mijatović, Sanja, Maksimović-Ivanić, Danijela, McCubrey, James A, "Sensitization of cancer stem cells based on inhibiting key signal transduction pathways" in International Journal of Molecular Medicine, 28, no. null (2011),
https://hdl.handle.net/21.15107/rcub_ibiss_1313 .

TY  - CONF
AU  - McCubrey, James A
AU  - Chappell, William H
AU  - Abrams, Stephen L
AU  - Martelli, Alberto M
AU  - Stivala, Franca
AU  - Nicoletti, Ferdinando
AU  - Fagone, Paolo
AU  - Mazzarino, Clorinda
AU  - Mulaponte, Graziella
AU  - Libra, Mussimo
AU  - Cervello, Melchiorre
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Steelman, Linda S
PY  - 2011
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1312
C3  - International Journal of Molecular Medicine
T1  - Novel approaches to target the prostate cancer stem cell - eliminating the root of the cancer
IS  - null
VL  - 28
EP  - S18
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1312
ER  - 

@conference{
author = "McCubrey, James A and Chappell, William H and Abrams, Stephen L and Martelli, Alberto M and Stivala, Franca and Nicoletti, Ferdinando and Fagone, Paolo and Mazzarino, Clorinda and Mulaponte, Graziella and Libra, Mussimo and Cervello, Melchiorre and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Steelman, Linda S",
year = "2011",
journal = "International Journal of Molecular Medicine",
title = "Novel approaches to target the prostate cancer stem cell - eliminating the root of the cancer",
number = "null",
volume = "28",
pages = "S18",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1312"
}

McCubrey, J. A., Chappell, W. H., Abrams, S. L., Martelli, A. M., Stivala, F., Nicoletti, F., Fagone, P., Mazzarino, C., Mulaponte, G., Libra, M., Cervello, M., Maksimović-Ivanić, D., Mijatović, S.,& Steelman, L. S.. (2011). Novel approaches to target the prostate cancer stem cell - eliminating the root of the cancer. in International Journal of Molecular Medicine, 28(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1312

McCubrey JA, Chappell WH, Abrams SL, Martelli AM, Stivala F, Nicoletti F, Fagone P, Mazzarino C, Mulaponte G, Libra M, Cervello M, Maksimović-Ivanić D, Mijatović S, Steelman LS. Novel approaches to target the prostate cancer stem cell - eliminating the root of the cancer. in International Journal of Molecular Medicine. 2011;28(null):null-S18.
https://hdl.handle.net/21.15107/rcub_ibiss_1312 .

McCubrey, James A, Chappell, William H, Abrams, Stephen L, Martelli, Alberto M, Stivala, Franca, Nicoletti, Ferdinando, Fagone, Paolo, Mazzarino, Clorinda, Mulaponte, Graziella, Libra, Mussimo, Cervello, Melchiorre, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Steelman, Linda S, "Novel approaches to target the prostate cancer stem cell - eliminating the root of the cancer" in International Journal of Molecular Medicine, 28, no. null (2011),
https://hdl.handle.net/21.15107/rcub_ibiss_1312 .

TY  - CONF
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Harhaji-Trajković, Ljubica
AU  - Miljković, Đorđe
AU  - Donia, Marco
AU  - Al-Abed, Yousef
AU  - Stivala, Franca
AU  - Mazzarino, Clorinda
AU  - Libra, Massimo
AU  - Nicoletti, Ferdinando
AU  - Stošić-Grujičić, Stanislava
PY  - 2007
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1618
C3  - Nitric Oxide-Biology and Chemistry
T1  - Novel NO-donation compound GIT-27NO possesses strong tumoricidal capacity in vitro and in vivo
IS  - null
VL  - 17
EP  - S25
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1618
ER  - 

@conference{
author = "Maksimović-Ivanić, Danijela and Mijatović, Sanja and Harhaji-Trajković, Ljubica and Miljković, Đorđe and Donia, Marco and Al-Abed, Yousef and Stivala, Franca and Mazzarino, Clorinda and Libra, Massimo and Nicoletti, Ferdinando and Stošić-Grujičić, Stanislava",
year = "2007",
journal = "Nitric Oxide-Biology and Chemistry",
title = "Novel NO-donation compound GIT-27NO possesses strong tumoricidal capacity in vitro and in vivo",
number = "null",
volume = "17",
pages = "S25",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1618"
}

Maksimović-Ivanić, D., Mijatović, S., Harhaji-Trajković, L., Miljković, Đ., Donia, M., Al-Abed, Y., Stivala, F., Mazzarino, C., Libra, M., Nicoletti, F.,& Stošić-Grujičić, S.. (2007). Novel NO-donation compound GIT-27NO possesses strong tumoricidal capacity in vitro and in vivo. in Nitric Oxide-Biology and Chemistry, 17(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1618

Maksimović-Ivanić D, Mijatović S, Harhaji-Trajković L, Miljković Đ, Donia M, Al-Abed Y, Stivala F, Mazzarino C, Libra M, Nicoletti F, Stošić-Grujičić S. Novel NO-donation compound GIT-27NO possesses strong tumoricidal capacity in vitro and in vivo. in Nitric Oxide-Biology and Chemistry. 2007;17(null):null-S25.
https://hdl.handle.net/21.15107/rcub_ibiss_1618 .

Maksimović-Ivanić, Danijela, Mijatović, Sanja, Harhaji-Trajković, Ljubica, Miljković, Đorđe, Donia, Marco, Al-Abed, Yousef, Stivala, Franca, Mazzarino, Clorinda, Libra, Massimo, Nicoletti, Ferdinando, Stošić-Grujičić, Stanislava, "Novel NO-donation compound GIT-27NO possesses strong tumoricidal capacity in vitro and in vivo" in Nitric Oxide-Biology and Chemistry, 17, no. null (2007),
https://hdl.handle.net/21.15107/rcub_ibiss_1618 .

TY  - CONF
AU  - Malaponte, Graziella
AU  - Libra, Massimo
AU  - Cardile, Vera
AU  - Lombardo, L
AU  - Ligresti, Giovanni
AU  - Mangano, Katia
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Al-Abed, Yousef
AU  - Mazzarino, Maria C
AU  - Nicoletti, Ferdinando
AU  - Stivala, Franca
PY  - 2007
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/1619
C3  - Nitric Oxide-Biology and Chemistry
T1  - GIT-27 NO may be a potential therapeutic agent for melanoma treatment by inhibition of the transcription repressor YIN-YANG
IS  - null
VL  - 17
EP  - S25
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_1619
ER  - 

@conference{
author = "Malaponte, Graziella and Libra, Massimo and Cardile, Vera and Lombardo, L and Ligresti, Giovanni and Mangano, Katia and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Al-Abed, Yousef and Mazzarino, Maria C and Nicoletti, Ferdinando and Stivala, Franca",
year = "2007",
journal = "Nitric Oxide-Biology and Chemistry",
title = "GIT-27 NO may be a potential therapeutic agent for melanoma treatment by inhibition of the transcription repressor YIN-YANG",
number = "null",
volume = "17",
pages = "S25",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_1619"
}

Malaponte, G., Libra, M., Cardile, V., Lombardo, L., Ligresti, G., Mangano, K., Maksimović-Ivanić, D., Mijatović, S., Al-Abed, Y., Mazzarino, M. C., Nicoletti, F.,& Stivala, F.. (2007). GIT-27 NO may be a potential therapeutic agent for melanoma treatment by inhibition of the transcription repressor YIN-YANG. in Nitric Oxide-Biology and Chemistry, 17(null).
https://hdl.handle.net/21.15107/rcub_ibiss_1619

Malaponte G, Libra M, Cardile V, Lombardo L, Ligresti G, Mangano K, Maksimović-Ivanić D, Mijatović S, Al-Abed Y, Mazzarino MC, Nicoletti F, Stivala F. GIT-27 NO may be a potential therapeutic agent for melanoma treatment by inhibition of the transcription repressor YIN-YANG. in Nitric Oxide-Biology and Chemistry. 2007;17(null):null-S25.
https://hdl.handle.net/21.15107/rcub_ibiss_1619 .

Malaponte, Graziella, Libra, Massimo, Cardile, Vera, Lombardo, L, Ligresti, Giovanni, Mangano, Katia, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Al-Abed, Yousef, Mazzarino, Maria C, Nicoletti, Ferdinando, Stivala, Franca, "GIT-27 NO may be a potential therapeutic agent for melanoma treatment by inhibition of the transcription repressor YIN-YANG" in Nitric Oxide-Biology and Chemistry, 17, no. null (2007),
https://hdl.handle.net/21.15107/rcub_ibiss_1619 .